FAM83D activates the MEK/ERK signaling pathway and promotes cell proliferation in hepatocellular carcinoma
FAM83D activates the MEK/ERK signaling pathway and promotes cell proliferation in hepatocellular carcinoma
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FAM83D 激活 MEK/ERK 信号通路并促进肝细胞癌细胞增殖
DOI：
10.1016/j.bbrc.2015.01.108
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发表时间：
2015-03-06
影响因子：
3.1
通讯作者：
Li, Xiang-Cheng
中科院分区：
文献类型：
--
作者：
Wang, Dong;Han, Sheng;Li, Xiang-Cheng
公开可用的微阵列数据表明，FAM 83 D（具有序列相似性的家族83，成员D）的表达在多种肿瘤类型中升高，包括肝细胞癌（HCC）。然而，其在HCC发病机制中的作用尚未阐明。在这里，我们发现FAM 83 D在HCC样品中频繁上调。FAM 83 D在肝癌细胞系中的强制表达显著促进其增殖和集落形成，而FAM 83 D敲低则导致相反的效果。机制分析表明，FAM 83 D能够激活MEK/ERK信号通路，促进细胞进入S期。综上所述，这些结果表明，FAM 83 D是一个新的癌基因在肝癌的发展，并可能构成一个潜在的治疗肝癌的目标。(C)2015 Elsevier Inc. All rights reserved.
Publicly available microarray data suggests that the expression of FAM83D (Family with sequence similarity 83, member D) is elevated in a wide variety of tumor types, including hepatocellular carcinoma (HCC). However, its role in the pathogenesis of HCC has not been elucidated. Here, we showed that FAM83D was frequently up-regulated in HCC samples. Forced FAM83D expression in HCC cell lines significantly promoted their proliferation and colony formation while FAM83D knockdown resulted in the opposite effects. Mechanistic analyses indicated that FAM83D was able to activate the MEK/ERK signaling pathway and promote the entry into S phase of cell cycle progression. Taken together, these results demonstrate that FAM83D is a novel oncogene in HCC development and may constitute a potential therapeutic target in HCC. (C) 2015 Elsevier Inc. All rights reserved.